YANG Juan , WANG Hong-Xin , ZHANG Ying-Jie , LI Sheng-Tao , LU Mei-Li , ZHANG Jing , ZHANG Su-Ping
Abstract:Aim To observe the effect of TLR4/NF-κB signaling pathway on astragaloside IV inhibiting myocardial hypertrophy induced by isoproterenol (ISO). Methods The ISO [5 mg/(kg·d)] was used as myocardial hypertrophy models by intraperitoneal injection. Sixty SD rats were randomly assigned to the following six groups (10 rats for each group): normal group, ISO group, ISO plus astragaloside IV 20 mg/(kg·d) group, ISO plus astragaloside IV 40 mg/(kg·d) group, ISO plus astragaloside IV 80 mg/(kg·d) group, ISO plus propranolol 40 mg/(kg·d) group. Administered groups received continually intragastric administration for 3 weeks, and ISO were intraperitoneal injected as long as 2 weeks in the day after that. 3 weeks later, heart mass index (HMI) and left ventricular mass index (LVMI) of rats in each group were measured. HE staining was used for measuring transverse diameter of left ventricular myocardial cells (TDM). RT-PCR was used to quantify mRNA expression of ANP and TLR4, Western blot was used to quantify protein expression of TLR4, p65 and IκBα in the tissue, ELISA was used to quantify TNF-α and IL-6. Results Comparing the ISO group with the normal group, the differences were in the followings: the HMI and LVMI were significantly increased, the TDM were increased, the protein expression of TLR4 and p65 were increased, while the IκBα were decreased the expression of TLR4 and ANP mRNA were increased, TNF-α and IL-6 in serum were significantly increased. Comparing the other 3 groups (ISO plus astragaloside IV) with the ISO group, the differences were in the followings: the HMI and LVMI were significantly decreased, TDM were decreased, the protein expression of TLR4 and p65 were decreased, while the IκBα were increased;the expression of TLR4 and ANP mRNA were decreased, TNF-α and IL-6 in serum were significantly decreased, and the differences were positively related to dose of three groups. Conclusions astragaloside IV has a protective effect on cardiac hypertrophy induced by ISO, which is partially referred to inhibiting the TLR4/NF-κB signaling pathway and more than attenuating inflammatory effect.
HUANG Xian-Sheng , WANG Ren , MA Xiao-Feng , CHEN Na-Ping , ZHANG Kai , WANG Zuo
Abstract:Aim To explore the effect of momordicin on nuclear translocation of inflammatory factor nuclear factor-kappa B (NF-κB) in ApoE-/- mice and further analyze the molecular mechanisms related to momordicin anti-inflammatory. Methods 40 male ApoE-/- mice, 6 weeks old, were randomly divided into four groups: normal food group, high fat high cholesterol group, high fat high cholesterol and momordicin group, normal food and momordicin group. After feeding 12 weeks, all mice were removed eyeball in order to obtain blood preparation. Level of inflammatory factors (IL-1β, TNF-α, IL-6, IFN-γ) and anti-inflammatory factors (IL-10) were measured by ELISA, IκB expression of aorta was analyzed by immunohistochemistry. Gene and protein expression was analyzed by semi-quantitative RT-PCR and Western blot, respectively. Results After fed with high fat high cholesterol about 12 weeks, inflammatory factors (IL-1β, TNF-α, IL-6, IFN-γ) level increased compared with normal food group(P<0.01, n5), but the level of IL-10 can not be up-regulated. After momordicin treating, inflammatory factors level decreased, yet IL-10 can not increase. Not only momordicin inhibited p65 mRNA transcription compared with high fat high cholesterol group, but also the nuclear level of NF-κB of momordicin treat group were obviously lower than high fat high cholesterol group in artery wall, nuclear translo cation of NF-κB was inhibited by momordicin treating. IκB in high fat high cholesterol group was remarkably reduced compared with normal food group (0.19±0.05 vs 0.74±0.15, P<0.05, n5), but this reduction can be obviously inhibited by momordicin intervention(0.19±0.05 vs 0.36±0.07, P<0.01,n5). Conclusions The role of momordicin anti-inflammatory factors generation is related to inhibiting degradation of IκB, which inhibits nuclear translocation of NF-κB.
SUN Jia-Yin , ZHAI Lin , LI Qiao-Ling , KANG Li-Na , XU Biao
Abstract:Aim To investigate the beneficial effects of amlodipine on neovascularization and cardiac function in rats after acute myocardial infarction (AMI), and explore the potential underlying mechanism for these effects. Methods Left anterior descending coronary artery ligation was performed to induce AMI. Rats post-AMI were randomly assigned into amlodipine group and control group after surgery (n20 in each group). Capillary density in the peripheral area of infarction and small artery density in myocardium were determined by CD31 and α-SMA staining separately. The percentage of CD45-/low+CD133+KDR+ EPC in peripheral blood mononuclear cells was measured by flow cytometry pre-operation and on day 7 post-operation. The expression and phosphorylation of protein associated with neovascularization in the border zone of infarction were determined by Western blot analysis. Echocardiagraphy was performed to evaluate cardiac function. Results Amlodipine treatment could notably increase the density of capillary vessels (81.3±4.0 vs 69.0±5.6, P<0.05) around infarction and small arteries (11.5±3.5 vs 6.2±2.3, P<0.05) in myocardium. At the same time, elevated circulating EPC count (120.3±18.3/106 vs 42.5±6.3/106, P<0.01) as well as increased expression of VEGF, phosphor-Akt, phosphor-eNOS and NO in the border zone of infarction (all P<0.05) were observed.
ZHAO Guo-Jun , TANG Shi-Lin , TIAN Guo-Ping , OUYANG Xin-Ping , LV Yun-Cheng , HE Ping-Ping ,
Abstract:Aim T0901317 is a synthetic liver X receptor (LXR) agonist. This study was to investigate the effects and potential mechanisms of T0901317 on proinflammatory cytokine release from lipopolysaccharide (LPS)-induced THP-1 macrophages. Methods Human THP-1 macrophages were induced using phorbol-12-myristate acetate (PMA, 160 nmol/L) for 24 h, then cells were divided into four groups: control group, LPS group, T0901317 group and LPS+T0901317 group. Secretion of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) was performed by enzyme-linked immunosorbent assay (ELISA). The siRNAs for ATP-binding cassette transporter A1 (ABCA1) were transfected into THP-1 macrophages by positive ion liposome LipofectamineTM2000. The mRNA expression of ABCA1, ABCG1 and Toll like receptor 4 (TLR4) were examined by real-time PCR analysis. The proteins expression of ABCA1, ABCG1, TLR4 and nuclear factor-κB (NF-κB) p65 were examined by Western blot. Results T0901317 inhibited the release of TNF-α, IL-6 and IL-1β induced by LPS, and promoted the expression of ABCA1 and ABCG1 on THP-1 macrophages. Transfection of ABCA1 siRNA significantly decreased the of expression ABCA1 protein and weakened the effect of T0901317 on the LPS-stimulated inflammatory response. Furthermore, T0901317 repressed the expression of TLR4 and the translocation of NF-κB to the nucleus. Conclusions T0901317 inhibited the release of inflammatory cytokine that induced by LPS, and the mechanisms may be related to promotion of membrane transporter ABCA1 expression and inhibition of membrane receptors TLR4 and the transcription factor NF-κB expression.
QIN Yu-Sheng , YANG Yu-Hong , LIANG Ling-Jun , SONG Ying , LI Hong-Xiu , WANG Hong-Xin
Abstract:Aim To explore effects and mechanism of panax notoginseng saponin (PNS) on hypertrophic myocardium caused by abdominal aorta constriction(AAC) in rats. Methods Rat left ventricular hypertrophy was induced by abdominal aorta constriction in 75 rats, and 15 rats were randomly taken as sham group. One week after surgery, rats were divided into 4 groups: model group (abdominal aorta constriction rats), low-dose PNS group (50 mg/kg), middle-dose PNS group (100 mg/kg) and high-dose PNS group (150 mg/kg). After accepting therapy for 11 weeks, the hemodynamics of all animals was detected the left ventricle was recorded to calculate left ventricular hypertrophic parameters including left ventricular hypertrophy index (HMI, the ratio of the heart and body weight and LVMI, the ratio of the left ventricular weight and body weight) pathological section was stained by hematoxylin-eosin(HE) the lactic acid (LAC) and free fatty acids(FFA) were measured the mRNA expression of heart atrial natriuretic peptide (ANP) was observed through reverse transcription-polymerase chain reaction (RT-RCR) the contents of adenosine triphosphate (ATP), adenosine diphosphate(ADP) and adenosine monophosphate (AMP) in rat were detected by high performance liquid chromatography (HPLC). Results Compared with the AAC model group, PNS was able to inhibit cardiac hypertrophy, ameliorate hemodynamics, the expression of atrial natriuretic peptide was decreased, the lactic acid (LAC) and free fatty acid (FFA) levels was decreased, and the content of ATP, ADP and AMP was largely increased. Conclusions PNS protection against left ventricular hypertrophy elicited by abdominal aorta constriction in rats is mediated, at least in part, via ameliorate energy metabolism.
HUANG Da , PAN Zheng , LAN Jing-Sheng , HE Jin-Long , WEI Bao-Min
Abstract:Aim To investigate the effects and mechanism of rosuvastatin on TGF-β1-induced proliferation and collagen synthesis in neonatal rat cardiac fibroblasts. Methods Cardiac fibroblasts of neonatal SD rats were isolated and cultured, effect of rosuvastatin on fibroblast proliferation was detected by CCK-8, collagen synthesis was measured with real time-PCR, collagen secretion was checked by ELISA, Akt protein expression was tested by Western blot. Results Rosuvastatin dose-dependently inhibited TGF-β1-induced cardiac fibroblast proliferation, collagen synthesis and collagen secretion, and rosuvastatin could also inhibit Akt activity. Conclusions Rosuvastatin may inhibit TGF-β1-induced cardiac fibrosis through inhibiting cardiac fibroblast proliferation, collagen synthesis and collagen secretion. Its molecular basis may be associated with inhibiting Akt signaling pathway.
WU Ya-Li , ZHOU Hong-Lian , ZHENG Hong-Bo , TONG Xue-Ying
Abstract:Aim To observe the expression of integrin β3 by making rat model of abdominal aortic aneurysm and explore the significance of integrin β3 in the pathogenesis of abdominal aortic aneurysm. Methods Making a rat model of abdominal aortic aneurysm and measuring the diameter of all aortas then calculating their extended rate of the aorta. HE staining was used to observe the change of pathology. Immunohistochemistry and real time PCR were used to detect the expression of integrin β3 from the level of protein and gene. Results Rat model of abdominal aortic aneurysm was successfully made. Compared with saline group and normal group(1.175±0.159 and 1), the extended rate of experimental group (3.689±0.443) was obviously rising and the infiltration of inflammatory cell was more apparent (P<0.05). Immunohistochemistry showed that the expression of integrin β3 in experimental group, saline group and normal group were 0.33±0.07,0.20±0.06 and 0.19±0.07 (P<0.05);Real time PCR showed the expression of integrin β3 mRNA in experimental group, saline group and normal group were 36.23±5.65, 1.14±0.30 and 1 (P<0.05). Conclusions The increasing expression of integrin β3 may participate in the occurrence and development of experimental abdominal aneurysms.
ZHONG Yong , PEI Ying-Hao , WANG Jun , GONG Jian-Bin , JIANG Shi-Sen
Abstract:Aim To identify a serum microRNA(miRNA) expression profile that can serve as a novel diagnostic biomarker for myocardial bridging (MB) detection. Methods Serum samples were taken from 100 MB patients and 50 controls. An initial screening of miRNA expression by microarray was performed using serum samples pooled from 20 MB patients and 10 controls, respectively. Differential expression was validated using hydrolysis probe-based stem-loop quantitative reverse transcription polymerase chain reaction (RT-qPCR) in individual samples. Results The microarray results demonstrated that 21 serum miRNAs were markedly different in the MB patients compared with the controls. The RT-qPCR analysis further identified a profile of four serum miRNAs (miR-92a, miR-487a, miR-29b and miR-126) as a biomarker for MB detection. The areas under the receiver operating characteristic (ROC) curve of this four-serum miRNAs were 0.998, 0.956, 0.719 and 0.986 respectively, and using the optimal cutoff value, we obtained the following sensitivity and specificity values to detect MB: 97% and 100%, 97% and 100%, 45.5% and 100%, 87.9% and 100% respectively. Conclusions We identified four serum miRNAs signature for MB diagnosis by genome-wide serum miRNA expression profiling. Expression levels of this serum miRNA may be a novel biomarker for early detection of MB in human.
XU Qin , ZHANG Wei-Wei , WEI Wei , HUANG Yong-Hua , WANG Guo-Qiang
Abstract:Aim To observe the relationship between carotid artery stenosis and stroke in progression(SIP), and further discuss the risk factors of SIP. Methods 239 hospitalized patients from the Beijing Military General Hospital with acute cerebral infarction were randomly allocated into two groups: stroke in progression(SIP) group(n141) and stable cerebral infarction group(n98). Carotid ultrasonography examination was performed. The plasma Hcy were determined by radio-immunofluo rescence. The carotid artery stenosis degree and the plasma homocysteine levels of two groups were compared. Results The incidence of carotid artery stenosis in progress group was obviously higher than stable cerebral infarction group. The carotid artery stenosis is associated with stroke in progression. Logistic regression analysis show that hyperlipemia, homocysteine, carotid artery stenosis were the independent risk factors to stroke in progression(OR0.264,95%CI:0.064~1.260OR0.163,95%CI:0.036~0.743OR0.006,95%CI:0.036~0.568). Conclusion Carotid artery stenosis may be closely related to ischemic stroke in progression, and the level of Hcy is a prediction of progressive cerebral infarction.
PAN Shao-Yi , LI Li-Hua , ZHANG Lei , YIN Xue-Yan
Abstract:Aim To explore the associations of angiotensin Ⅱ type 1 receptor (AT1R) A1166C variant with blood pressure in Chinese. Methods We invited all unrelated employees and retired workers to take part in this study, and 1466 participants were included in the present analysis. Standardized questionnaires were used to collect information on alcohol consumption, smoking habits, and use of medications. The AT1R genotype was determined by SNaPshot method. Results One thousand four hundred and sixty six participants included 566 (37.9%) women, 485 (33.1%) overweight/obese participants, 468 (31.9%) hypertensive patients, of whom 212 (45.3%) took antihypertensive treatment. The frequencies of AA, CA and CC were 90.5%, 9.4% and 0.1%, respectively. There was no significant difference in the distributions of genotypes and alleles between participants with normal blood pressure and hypertensive patients (P>0.05). Furthermore, there was no significant difference in systolic and diastolic blood pressure and pulse pressure between genotypes before and after adjusted for covariates (P>0.05). We found significant interaction between the A1166C variant and body mass index on systolic blood pressure (Pint=0.002) and pulse pressure (Pint=0.02). Only among participants in the highest quartile of body mass index (>25.8 kg/m2), C allele carriers had significantly higher systolic blood pressure (P=0.02) and pulse pressure (P=0.009) than AA homozygotes. Conclusions Significant interactions were observed between AT1R A1166C variant and body mass index on systolic blood pressure and pulse pressure.
FANG Ye-Qing , XIE Xiu-Mei , XIE Pei-Yi , SU You-Su , FANG Hong-Cheng
Abstract:Aim To study the change of EPC and expression of its tPA and PAI in patients with coronary heart disease. Methods EPC isolated from peripheral blood of patients with coronary heart diseases(n57) and control (n30) were cultured and tPA and PAI in the supernatant were determined by ELISA and Substrate chemiluminescence.The expression of tPA mRNA and PAI mRNA were detected by RT-PCR. Results The number of EPC was significantly reduced in patients with CAD compared with control subjects. The cell colony forming was also decreased in patients with CAD. The concentration and activity of EPC patients with CAD were lower than EPC of control group. The tPA mRNA expression, the concentration and activity of EPC had degression tendency in patients with coronary heart diseases, and PAI displayed opposite tendency. Conclusion The number of EPC were decreased and their function were impaired in patients with CAD, which may play an important role in the initiation and progression of CAD.
ZHANG Zi-Xin , LI Chao-Jun , YU Lu-Jiao
Abstract:Aim To investigate the association of endothelial microparticle (EMP) and brachial-ankle pulse wave velocity (baPWV) in patients with stable coronary artery disease (CAD). Methods 50 patients with stable coronary artery disease and 20 healthy volunteers were studied. Flow cytometer was used to measure levels of EMP (CD31+/CD42b-) in circulation and baPWV was measured to assess the status of arterial elasticity. Results The levels of EMP were higher in patients with stable CAD than that of healthy volunteers (1 748.4±102.1 particles/μL vs 847.4±86.4 particles/μL, P<0.01), and baPWV was faster in patients with stable CAD than that of healthy volunteers (1 931.1±328.3 cm/s vs 1 532.1±147.3 cm/s, P<0.01). There was a positive correlation between the level of EMP and baPWV in stable CAD (r=0.42, P<0.01). Conclusions Patients with stable CAD had higher EMP and faster baPWV than those of healthy volunteers, and there was positive correlation between EMP and baPWV. EMP was an independent influencing factor to arterial elasticity.
LI Qing-Xiang , ZHANG Ying , ZHU Xiao-Ling
Abstract:Aim To investigate the incidence and risk factor of coronary heart disease complicated with non-alcoholic fatty liver disease (NAFLD) in patients undergoing coronary angiogram. Methods 1346 patients with coronary heart disease who underwent coronary angiogram were enrolled into this study. All patients had ultrasound screening for fatty liver. Results Among 612 recruited patients, 678 (50.4%5) had fatty liver by ultrasonography. Incidence of NAFLD in the patients in 3-vessel disease was higher than those of 1, 2-vessel disease (P<0.01). By multivariable Logistic regression analysis, diabetes mellitus, multi-vessel lesions or stenosis of left main stem were risk factors in NAFLD patients with coronary heart disease. Conclusion In coronary heart disease patients, increase in the incidence of NAFLD were related to coronary atherosclerosis severity aggravating, especially the patients with diabetes mellitus.
DONG Dan-Hong , SONG Jie , ZHENG Hong-Yan , QIU Ma-Li , SUN Guang-Hao , ZHANG Kui , ZHANG Chun-Lei , XU Biao
Abstract:Aim To observe the effect of CYP2C19 681G>A and 636G>A (CYP2C19*2 and *3) polymorphisms on residual platelet reactivity and adverse clinical events in clopidogrel-treated survivors after percutaneous coronary intervention (PCI). Methods 202 patients with coronary heart disease who received PCI and treated with clopidogrel were enrolled in our study from Jun 2011 to Dec 2011. Based on the number of the CYP2C19 mutation allele, patients were divided into normal group(n78, CYP2C19 *1/*1), one mutation allele group(n100, CYP2C19 *1/*2、CYP2C19 *1/*3) and two mutation alleles group(n24, CYP2C19 *2/*2、CYP2C19 *2/*3). Baseline data, residual platelet reactivity, major adverse cardiac events and bleeding within half a year were observed. Results There was no significant difference on baseline data among the groups besides Calcium channel blocker (normal group, one mutation allele group, two mutation alleles group: 15.4%, 29.0% and 45.8%, P0.007). Adenosine diphosphate induced platelet aggregations had no difference among all groups,no matter within 5 days(normal group, one mutation allele group, two mutation alleles group: 51.60%±17.21%, 55.89%±14.92% and 62.00%±9.75%, P0.060) or 3 months(normal group, one mutation allele group, two mutation alleles group: 49.45%±16.90%, 55.98%±19.03%, 57.64%±18.42%, P0.248). The incidence of nonfatal myocardial infarction was higher in two mutation alleles group than the other groups(normal group, one mutation allele group, two mutation alleles group: 0%, 0% and 8.3%, P0.001) whereas, the incidence of angina recurrence, stent thrombosis, acute heart failure, cardiac death and the bleeding had no difference among all groups. Conclusion Among the patients who received PCI and treated with clopidogrel, CYP2C19 681G>A and 636G>A polymorphisms appear to affect prophase residual platelet reactivity and cardiovascular events.
WANG Yin-Qian , XU Bo , ZHANG Xiang-Yang
Abstract:Aim To study the relationship between coronary heart disease and pregnancy-associated plasma protein A (PAPP-A) for guiding the clinical work. Methods The articles relating to the analysis of coronary heart disease and pregnancy-associated plasma protein A (PAPP-A) were studied from the China Journal Full-text Database and Pubmed professional foreign language database collected from 2001 to 2012. The right articles were chosen and analyzed with RevMan 5.0 software.Results This article encompasses 10 studies, including 1091 objects of study. The results show that: The relationship between the stable angina and PAPP-A levels is 95% CI 0.02, 0.34 (P=0.03) The relationship between unstable angina and PAPP-A levels is 95% CI 1.32, 1.74 (P<0.01) The relationship between acute myocardial infarction and PAPP-A levels is 95% CI 1.83, 2.38 (P<0.01). And the relationship between one coronary artery disease and PAPP-A levels is 95% CI 1.78, 2.50 (P<0.01) for two coronary arteries disease, it is 95% CI 1.83, 7.72 (P<0.01) for three coronary arteries disease, it is 95% CI 2.39, 3.26 (P<0.01). According to all these results of the study, it shows that the mutation quantity of coronary heart disease and coronary artery is highly connected with pregnancy associated plasma protein-A. And its of significance to statistics study. Conclusion Through the study, it shows that the quantity of coronary heart disease and coronary artery lesion has close relationships with pregnancy-associated plasma protein A.
ZHANG Lin-Ye , FANG Wu-Wang , BO Zhan , WANG Zong-Fang , YANG Yang
Abstract:Aim To evaluate the efficacy and safety of the application of tirofiban in acute ST-segment elevation myocardial infarction (STEMI) patients before percutaneous coronary intervention (PCI) treatment. Methods We performed systematic searches of MEDLINE, EMBASE, and CENTRAL databases for randomized controlled trials (RCT) of tirofiban use in STEMI patients treated with aspirin and clopidogrel which reported clinical outcomes after primary PCI.Statistical analysis was conducted with RevMan 5.0. Results Four randomized controlled trials were eligible for the inclusion, involving 811 patients in tirofiban group and 813 control subjects. The application of PCI, prior to the treatment of STEMI, the routine use of tirofiban major adverse cardiovascular events (MACE) within 30 days decreased (RR=0.63, 95%CI was 0.44~0.90, P=0.001) all-cause mortality incidences declined (RR=0.61, 95%CI was 0.35~1.05, P=0.007) re-myocardial infarction incidences were not significantly different between the two groups (RR=0.67, 95%CI was 0.34~1.31, P=0.24) there were no significant differences in the incidences of serious bleeding (RR=1.21, 95%CI was 0.67~2.16, P=0.53). Conclusions Current analysis of available studies suggests that routine and early tirofiban use before primary PCI may decrease the major cardiovascular events within 30 days in STEMI patients treated with aspirin and clopidogrel without any significant increase in major bleeding.
HUO Xiao-Chuan , GUAN Ning , FENG Xu , WANG Chao , ZHEN Wei , LUO Jun-Sheng
Abstract:Accumulation of cholesteryl ester (CE) stored as cytoplasmic lipid droplets is the main characteristic of macrophage foam cells. It is central to the development of atherosclerotic plaques. Since only unesterified or free cholesterol (FC) can be effluxed from the cells to extracellular cholesterol acceptors, hydrolysis of CE is the obligatory first step in CE mobilization from macrophages. This reaction, catalyzed by neutral cholesteryl ester hydrolase (CEH), is increasingly being recognized as the rate-limiting step in FC efflux. CEH, therefore, regulates the process of reverse cholesterol transport and ultimate elimination of cholesterol from the body. In this review, we discussed the characteristics of the various candidates recognized to date and examined their roles in hydrolyzing cellular CE and thus regulating atherogenesis. We aim to provide clues for using hydrolase as a therapeutic target for atherosclerosis.
Abstract:Studies have shown that exercise improves cardiovascular function in both animals and human. The underlying mechanisms of exercises effects on improvement of vascular function were discussed here, mainly focusing on aspects including exercises effects on vascular branch, endothelial function, and coronary atherosclerosis disease, in order to provide theoretical evidence for the prevention and therapy of vascular diseases.
GUO Yuan , YANG Tian , XU Dan-Yan , ZHAO Shui-Ping
Abstract:Nowadays, the measures of cardiac rehabilitation are consistently updated, but its utilization relatively lags behind, especially in our country, which presents a situation of clinical medicine advancing rapidly while rehabilitation medicine developing insufficiently. Generally speaking, the benefit of cardiac rehabilitation is significant and lasting, both for the whole society and the individuals. This article analyzes the latest measures of cardiac rehabilitation and its current developing situation.
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